Cancer pathogenesis and therapy最新文献

英文中文

Pan-cancer gene signature analysis of macrophage polarization and compound prediction for reprogramming tumor-associated macrophages toward M1-like macrophages 巨噬细胞极化泛癌基因特征分析及肿瘤相关巨噬细胞向m1样巨噬细胞重编程的化合物预测

IF 2.8

Cancer pathogenesis and therapy

Pub Date : 2025-05-20 DOI: 10.1016/j.cpt.2025.05.002

Xiaojing Liu , Cheng Liu , Yuting Jin , Jing Xu , Chunyan Xu , Wei Zhu

Background

Resting tumor-associated macrophages (TAMs) are stimulated by the tumor microenvironment and can be primarily polarized into two subtypes: M1-and M2-like. M1-like TAMs promote inflammation and eradicate tumor cells, whereas M2-like TAMs suppress inflammation and facilitate tumor development. However, the mechanisms underlying phenotypic switching in these macrophages remain unclear. Therefore, we aimed to characterize the gene expression profiles of M1-like and M2-like TAMs in pan cancers.

Methods

Three computational methods were used to estimate the infiltration score of TAMs in 9239 tumor samples across 31 solid cancer types, based on RNA sequencing databases. Tumor samples were divided into high- and low-score groups based on the median M1/M2 ratio. Furthermore, gene enrichment, protein interactions, and transcription factors were analyzed. Multiple pharmaco–omics profiles were used to identify potential drugs. Finally, binding between the compounds and drug targets was validated using molecular docking.

Results

Of the top 100 dysregulated genes in each cancer type, 70 and 82 genes with upregulated and downregulated expression, respectively, were consistently differentially expressed. We identified candidate drugs targeting protein phosphatase 2A (PP2A), a core protein. These included efaproxiral, hesperidin, ezetimibe, calcitriol, and linopirdine.

Conclusions

This study provides a pan-cancer characterization of the TAM polarization-related gene profile. Network pharmacology and molecular docking analyses revealed five promising therapeutic agents for TAM reprogramming. Thus, our findings provide valuable insights into the enhancement of immune responses to inhibit tumor immune escape and metastasis.

背景：肿瘤相关巨噬细胞（tam）受到肿瘤微环境的刺激，可分化为两种亚型：m1和m2样。m1样tam促进炎症并根除肿瘤细胞，而m2样tam抑制炎症并促进肿瘤发展。然而，这些巨噬细胞表型转换的机制尚不清楚。因此，我们旨在表征泛癌中m1样和m2样tam的基因表达谱。方法基于RNA测序数据库，采用3种计算方法对31种实体癌9239例肿瘤样本的tam浸润评分进行估算。根据中位M1/M2比值将肿瘤样本分为高分组和低分组。此外，还分析了基因富集、蛋白质相互作用和转录因子。多种药物组学资料被用来鉴定潜在的药物。最后，利用分子对接验证化合物与药物靶点之间的结合。结果在各肿瘤类型的前100个异常表达基因中，分别有70个和82个表达上调和下调的基因持续差异表达。我们确定了靶向蛋白磷酸酶2A （PP2A）的候选药物，这是一种核心蛋白。这些药物包括依法普罗韦、橙皮苷、依泽替米贝、骨化三醇和利诺匹定。结论本研究提供了TAM极化相关基因谱的泛癌特征。网络药理学和分子对接分析揭示了5种有前景的TAM重编程治疗药物。因此，我们的研究结果为增强免疫反应以抑制肿瘤免疫逃逸和转移提供了有价值的见解。

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引用次数: 0

Trastuzumab deruxtecan in advanced breast cancer patients with brain metastases or leptomeningeal metastases 曲妥珠单抗在晚期乳腺癌脑转移或脑脊膜转移患者中的应用

IF 2.8

Cancer pathogenesis and therapy

Pub Date : 2025-05-19 DOI: 10.1016/j.cpt.2025.05.003

Jinsong Liu , Liuliu Quan , Die Sang , Xiao Guan , Min Dou , Jian Yue , Peng Yuan

引用次数: 0

Commentary on the “Relationship between visceral obesity and prognosis in patients with stage IVB cervical cancer receiving radiotherapy and chemotherapy” 《IVB期宫颈癌放化疗患者内脏肥胖与预后的关系》述评

Cancer pathogenesis and therapy

Pub Date : 2025-05-01 DOI: 10.1016/j.cpt.2025.03.001

Gnanaprakash Jeyaraj

引用次数: 0

Claudin-9 (CLDN9) promotes gastric cancer progression by enhancing the glycolysis pathway and facilitating PD-L1 lactylation to suppress CD8+ T cell anti-tumor immunity CLDN9通过增强糖酵解途径，促进PD-L1乳酸化，抑制CD8+ T细胞抗肿瘤免疫，从而促进胃癌进展

Cancer pathogenesis and therapy

Pub Date : 2025-05-01 DOI: 10.1016/j.cpt.2024.09.006

Xingbin Hu , Wenhao Ouyang , Haizhu Chen , Zhihong Liu , Zijia Lai , Herui Yao

Background

Gastric cancer (GC) is a common malignancy characterized by the absence of reliable prognostic indicators and effective therapeutic targets. Claudin-9 (CLDN9) has been demonstrated to be upregulated in various cancers. However, its prognostic value, biological function, and regulatory mechanisms in GC remain unclear. Therefore, this study aimed to elucidate the role of CLDN9 in GC progression and its underlying mechanisms.

Methods

We utilized consensus cluster, random survival forest, and multivariate Cox regression analyses to identify CLDN9 in GC. Subsequently, we evaluated the mRNA and protein levels of CLDN9 in GC using quantitative real-time polymerase chain reaction (PCR) (qRT-PCR), Western blotting (WB), and immunohistochemistry (IHC). Furthermore, the role of CLDN9 in GC progression was investigated using a series of functional in vivo and in vitro experiments. Finally, we elucidated the molecular mechanisms of CLDN9 using bioinformatics, molecular biology, animal models, and patient tissue specimens.

Results

Two GC subtypes with survival and functional differences were identified based on glycolytic metabolic genes in the Cancer Genome Atlas (TCGA)- Stomach adenocarcinoma (STAD) dataset. A prognostic risk score was calculated using seven genes to assess the overall survival (OS) in GC. Using random survival forest and multivariate Cox analyses, we identified CLDN9 as the key gene linked to the glycolytic subtype and prognosis of GC. CLDN9 expression was significantly upregulated in patients with GC as well as in GC cells. CLDN9 knockdown inhibited tumor proliferation, invasion, and metastasis both in vivo and in vitro. Mechanistically, CLDN9 was found to regulate lactate dehydrogenase A (LDHA) expression and promote glycolytic metabolism by activating the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/hypoxia-inducible factor 1-alpha (HIF1α) signaling pathway. Additionally, lactate, a glycolytic metabolite, enhanced programmed cell death ligand 1 (PD-L1) lactylation and stability, which suppressed anti-tumor immunity in CD8⁺ T cells, thereby contributing to GC progression.

Conclusions

CLDN9 expression is associated with GC development and progression. Mechanistically, CLDN9 enhances the glycolysis pathway and facilitates PD-L1 lactylation through the PI3K/AKT/HIF1α signaling pathway, thereby suppressing anti-tumor immunity in CD8⁺ T cells. CLDN9 has the potential to serve as a novel prognostic marker and therapeutic target for GC.

胃癌是一种常见的恶性肿瘤，其特点是缺乏可靠的预后指标和有效的治疗靶点。Claudin-9 （CLDN9）已被证实在多种癌症中上调。然而，其在胃癌中的预后价值、生物学功能和调节机制尚不清楚。因此，本研究旨在阐明CLDN9在GC进展中的作用及其潜在机制。方法采用一致聚类分析、随机生存森林分析和多变量Cox回归分析对GC中的CLDN9进行鉴定。随后，我们使用定量实时聚合酶链反应（PCR）（qRT-PCR）、Western blotting （WB）和免疫组织化学（IHC）评估GC中CLDN9的mRNA和蛋白水平。此外，通过一系列体内和体外功能实验研究了CLDN9在GC进展中的作用。最后，我们利用生物信息学、分子生物学、动物模型和患者组织标本阐明了CLDN9的分子机制。结果基于癌症基因组图谱(TCGA)-胃腺癌（STAD）数据集中的糖酵解代谢基因，鉴定出两种存在生存和功能差异的GC亚型。采用7个基因计算预后风险评分，评估GC患者的总生存期（OS）。通过随机生存森林和多变量Cox分析，我们发现CLDN9是与GC糖酵解亚型和预后相关的关键基因。CLDN9在胃癌患者和胃癌细胞中的表达均显著上调。CLDN9敲低抑制肿瘤在体内和体外的增殖、侵袭和转移。在机制上，CLDN9通过激活磷脂酰肌醇3-激酶(PI3K)/蛋白激酶B (AKT)/缺氧诱导因子1- α (HIF1α)信号通路调节乳酸脱氢酶A （LDHA）表达，促进糖酵解代谢。此外，乳酸，一种糖酵解代谢物，增强程序性细胞死亡配体1 （PD-L1）的乳酸化和稳定性，从而抑制CD8+ T细胞的抗肿瘤免疫，从而促进GC的进展。结论scldn9的表达与胃癌的发生发展有关。在机制上，CLDN9通过PI3K/AKT/HIF1α信号通路增强糖酵解途径，促进PD-L1的乳酸化，从而抑制CD8+ T细胞的抗肿瘤免疫。CLDN9有潜力作为胃癌的一种新的预后标记物和治疗靶点。

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引用次数: 0

Erratum to “Integrative analysis of cuproptosis-related lncRNAs: Unveiling prognostic significance, immune microenvironment, and copper-induced mechanisms in prostate cancer” [Cancer Pathog Ther, 3 (2025):48–59] “铜中毒相关lncrna的综合分析：揭示前列腺癌预后意义、免疫微环境和铜诱导机制”[癌症病理学杂志，3 (2025):48-59]

Cancer pathogenesis and therapy

Pub Date : 2025-05-01 DOI: 10.1016/j.cpt.2025.01.004

Haitao Zhong , Yiming Lai , Wenhao Ouyang , Yunfang Yu , Yongxin Wu , Xinxin He , Lexiang Zeng , Xueen Qiu , Peixian Chen , Lingfeng Li , Jie Zhou , Tianlong Luo , Hai Huang

引用次数: 0

New advances in lung cancer treatment: Efficacy, safety, and future research directions 肺癌治疗的新进展：疗效、安全性及未来研究方向

Cancer pathogenesis and therapy

Pub Date : 2025-05-01 DOI: 10.1016/j.cpt.2024.09.005

Yintao Li, Jianxin Xue, Li Zhang

引用次数: 0

Cover 封面

Cancer pathogenesis and therapy

Pub Date : 2025-05-01 DOI: 10.1016/S2949-7132(25)00038-2

引用次数: 0

The latest research on advanced gynecological oncology: A therapeutic perspective 高级妇科肿瘤学的最新研究：治疗视角

Cancer pathogenesis and therapy

Pub Date : 2025-05-01 DOI: 10.1016/j.cpt.2024.08.003

Bohao Zheng , Jinlu Ma , Shengtao Zhou

引用次数: 0

Epithelial–mesenchymal transition (EMT) and its role in acquired epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) chemoresistance in non-small cell lung cancer (NSCLC) 上皮-间质转化（EMT）及其在非小细胞肺癌（NSCLC）获得性表皮生长因子受体-酪氨酸激酶抑制剂（EGFR-TKI）化疗耐药性中的作用

Cancer pathogenesis and therapy

Pub Date : 2025-05-01 DOI: 10.1016/j.cpt.2024.07.001

Ma. Carmela P. Dela Cruz, Paul Mark B. Medina

Epithelial–mesenchymal transition (EMT) is a biological process that involves the transformation of epithelial cells into cells with a mesenchymal phenotype, enhancing their migratory and invasive capabilities. EMT is crucial in embryonic development, tissue healing, and wound repair, and aids in forming diverse cell types and structures. However, aberrant EMT is involved in pathogenic processes, including fibrosis, cancer development, and progression. Recent studies show that EMT contributes to resistance to cancer treatment, including epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) therapy in non-small cell lung cancer (NSCLC). This review discusses the intricate relationship between EMT and acquired chemoresistance to EGFR-TKIs. It details evidence on how EGFR-TKIs might induce EMT and how EMT may cause EGFR-TKI resistance. Understanding these pathways is crucial for developing effective prognostic and therapeutic strategies to predict and combat acquired chemoresistance in NSCLC, advancing the field toward more targeted and personalized treatment approaches.

上皮-间充质转化（epithelial - mesenchymal transition， EMT）是上皮细胞向间充质表型细胞转化，增强其迁移和侵袭能力的生物学过程。EMT对胚胎发育、组织愈合和伤口修复至关重要，并有助于形成多种细胞类型和结构。然而，异常的EMT参与致病过程，包括纤维化、癌症的发生和进展。最近的研究表明，EMT有助于抵抗癌症治疗，包括非小细胞肺癌（NSCLC）的表皮生长因子受体-酪氨酸激酶抑制剂（EGFR-TKI）治疗。本文综述了EMT与EGFR-TKIs获得性化疗耐药之间的复杂关系。它详细介绍了EGFR-TKI如何诱导EMT以及EMT如何引起EGFR-TKI耐药性的证据。了解这些途径对于制定有效的预后和治疗策略来预测和对抗NSCLC的获得性化疗耐药至关重要，从而推动该领域朝着更有针对性和个性化的治疗方法发展。

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引用次数: 0

Spices and culinary herbs for the prevention and treatment of breast cancer: A comprehensive review with mechanistic insights 用于预防和治疗乳腺癌的香料和烹饪草药：从机理角度全面审视

Cancer pathogenesis and therapy

Pub Date : 2025-05-01 DOI: 10.1016/j.cpt.2024.07.003

Md. Liakot Ali, Fabiha Noushin, Qurratul Ain Sadia, Afroz Fathema Metu, Jannatul Naima Meem, Md. Tanvir Chowdhury, Md. Hossain Rasel, Khurshida Jahan Suma, Md. Abdul Alim, Muhammad Abdul Jalil, Md. Jahirul Islam Mamun, Md. Mahmudul Hasan, Neamul Hoque, Eva Azme

Breast cancer (BC) continues to be the primary malignant neoplasm affecting women. For many years, traditional approaches such as chemotherapy, hormone therapy, radiation, and surgical interventions have been employed to treat BC. However, these therapies often fall short due to considerable adverse effects and the development of multidrug resistance or tolerance. Spices and culinary herbs that have been utilized in culinary practices for millennia have also demonstrated therapeutic effects in traditional medicinal practices serving to both prevent and treat BC. This review aims to comprehensively explore the roles and underlying mechanisms through which spices and culinary herbs exert anti-BC properties. These natural ingredients exhibit diverse anti-BC effects that encompass diverse mechanisms, including the inhibition of BC cell proliferation, migration, metastasis, and angiogenesis, as well as the induction of cell cycle arrest and apoptosis. These actions are achieved by targeting signaling pathways such as phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR), notch signaling, Hedgehog signaling, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and Wingless/int (Wnt)/β-catenin signaling pathways that are predominantly overexpressed in breast tumors or are exploited by them to promote cancer progression. Additionally, compounds such as curcumin, allicin, gingerol, zerumbone, diosgenin, capsaicin, piperine, quercetin, malabaricone C, eugenol, cardamomin, carnosol, cinnamaldehyde, sinigrin present in these spices and herbs may be more effective with reduced side effects against BC compared to conventional chemotherapeutic drugs. This review presents a concise overview of the potential contributions of spices, culinary herbs, and their potent bioactive constituents against BC, with particular emphasis on elucidating their mechanisms of action.

乳腺癌（BC）仍然是影响妇女的主要恶性肿瘤。多年来，传统的方法，如化疗、激素治疗、放疗和手术干预已被用于治疗BC。然而，由于相当大的副作用和多药耐药或耐受性的发展，这些疗法往往达不到预期的效果。香料和烹饪草药已经在烹饪实践中使用了几千年，在传统医学实践中也证明了预防和治疗BC的治疗效果。本文旨在全面探讨香料和烹饪草药发挥抗bc作用的作用及其机制。这些天然成分表现出多种抗BC作用，包括多种机制，包括抑制BC细胞增殖、迁移、转移和血管生成，以及诱导细胞周期阻滞和凋亡。这些作用是通过靶向信号通路实现的，如磷酸肌肽3激酶(PI3K)/蛋白激酶B (Akt)/哺乳动物雷帕霉素靶蛋白（mTOR）、notch信号、Hedgehog信号、活化B细胞的核因子κ轻链增强子（NF-κB）和无翼/int (Wnt)/β-catenin信号通路，这些信号通路在乳腺肿瘤中主要过度表达或被它们利用来促进癌症进展。此外，与传统化疗药物相比，这些香料和草药中的化合物，如姜黄素、大蒜素、姜辣素、零骨、薯蓣皂苷元、辣椒素、胡椒碱、槲皮素、马来酸酮C、丁香酚、小豆蔻素、鼠油醇、肉桂醛、紫荆素等，可能对BC更有效，副作用更小。这篇综述简要介绍了香料、烹饪草药及其有效的生物活性成分对BC的潜在贡献，并特别强调了它们的作用机制。

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